As the retinoid-related receptor function regulating agents, compounds described in the following references are known.
(1) WO 00/01679 describes, as a retinoid-related receptor function regulating agent, a 1,3-azole derivative represented by the formula:
wherein R1 is an optionally substituted aromatic hydrocarbon group or an optionally substituted aromatic heterocyclic group; R2 is a hydrogen atom or an optionally substituted hydrocarbon group; X is O, S or a group of the formula: —NR4— (R4 is a hydrogen atom or an optionally substituted alkyl group); A is an optionally substituted aromatic hydrocarbon group or an optionally substituted aromatic heterocyclic group; and R3 is a group of the formula: —OR5 (R5 is a hydrogen atom or an optionally substituted hydrocarbon group) or —NR6R7 (R6 and R7 are the same or different and each is a hydrogen atom or an optionally substituted hydrocarbon group, R6 and R7 may form a ring together with the adjacent nitrogen atom).
(2) WO 97/34869 describes, as a pharmaceutical agent having retinoic acid receptor agonism, a fused ring-containing carboxylic acid derivative represented by the formula:
wherein  is a single bond or a double bond, in the formula, X, Y, Z, P, Q, U, V and W are each a group of the formula: —O—, a group of the formula: —S— or a group of the formula:
wherein Rk (k: 1–8) is a hydrogen atom, a halogen atom, a lower alkyl group optionally having substituents and the like, and one of R7 and R8 is a group of the formula:
(ring A and ring B are each independently an aromatic hydrocarbon ring or unsaturated heterocycle, each of which optionally has substituents, and D is a carboxyl group optionally having a protecting group).
(3) WO 97/02244 describes, as a new retinoid-related compound replacing retinoic acid, a heterocycle containing carboxylic acid derivative represented by the formula: A-B-(D)n1-(C═O)-M wherein A is a heteroaryl group which has at least one nitrogen atom and optionally has substituents, and the like, B is a heteroarylene group, a group of —CONH—, a group of —CR6═CR7— (R6 and R7 are each H, a lower alkyl group etc.), and the like, D is an arylene group, a heteroarylene group and the like, n1 is 0 or 1, M is a hydroxyl group, a lower alkoxy group and the like.
Peroxisome proliferator-activated receptor gamma (PPARγ), a member of the intranuclear hormone receptor superfamily, which is typically exemplified by steroid hormone receptors and thyroid hormone receptors, plays an important role as a master regulator in the differentiation of adipocytes with its expression induced in the very early stage of adipocyte differentiation. PPARγ forms a dimer with retinoid X receptor (RXR) by binding to a ligand, and binds to a responsive site of the target gene in the nucleus to directly control (activate) transcription efficiency. In recent years, the possibility that 15-deoxy-Δ12.14 prostaglandin J2, which is a metabolite of prostaglandin D2, serves as an endogenous ligand for PPARγ, has been suggested, and it has been shown that a class of insulin sensitizers, typically exemplified by thiazolidinedione derivatives, possess ligand activity for PPARγ, and that its potency is proportional to its glucose-lowering action or adipocyte differentiation-promoting action [Cell, vol. 83, p. 803 (1995); The Journal of Biological Chemistry, vol. 270, p. 12953 (1995); Journal of Medicinal Chemistry, vol. 39, p. 655 (1996)]. Furthermore, in recent years, it has been shown that 1) PPARγ is expressed in cultured cells of human liposarcoma origin, whose proliferation is ceased by the addition of a PPARγ ligand [Proceedings of the National Academy of Sciences of the United States of America, vol. 94, p. 237 (1997)], 2) nonsteroidal anti-inflammatory drugs, typically exemplified by indomethacin and fenoprofen, have PPARγ ligand activity [The Journal of Biological Chemistry, vol. 272, p. 3406 (1997)], 3) PPARγ is expressed at high levels in activated macrophages, with the transcription of a gene involved in inflammation inhibited by the addition of a ligand therefor [Nature, vol. 391, p. 79 (1998)], and 4) PPARγ ligands suppress the production of inflammatory cytokines (TNFα, IL-1β, IL-6) by monocytes [Nature, vol. 391, p. 82 (1998)] and the like.